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Background: There are multiple treatment methods for odontogenic sinusitis (OS); however, the optimal treatment remains unclear., Aims/objective: To determine the cure rate of OS after tooth extraction and the factors contributing to the cure., Material and Methods: We prospectively identified 37 patients diagnosed with OS with an indication for causative tooth extraction. Before and three months after tooth extraction, the patients were assessed using sinus computed tomography and classified as either cured or uncured based on the absence or presence of soft tissue shadow in the maxillary sinus. The prognostic factors were analysed by comparing the two groups., Results: There were ten patients for whom all data could be obtained. The mean age of the patients at the time of tooth extraction was 53.8 ± 12.9 years (range, 34-75 years). In seven patients, the soft tissue shadow in the maxillary sinus disappeared; these patients were classified as cured. Uncured patients were significantly younger than cured patients (59.9 vs. 39.7 years)., Conclusions and Significance: Tooth extraction effectively treated OS in 70% of patients. However, even after tooth extraction, OS may not improve, particularly in younger patients.

The suprachiasmatic nucleus (SCN) is the master circadian clock in mammals and is properly entrained by environmental light cycle. However, the molecular mechanism(s) determining the magnitude of phase shift by light is still not fully understood. The orphan G-protein-coupled receptor Gpr176 is enriched in the SCN, controls the pace (period) of the circadian rhythm in behavior but is not apparently involved in the light entrainment; Gpr176 -/- animals display a shortened circadian period in constant darkness but their phase-resetting responses to light are normal. Here, we performed microarray analysis and identified enhanced mRNA expression of neuromedin U (Nmu) and neuromedin S (Nms) in the SCN of Gpr176 -/- mice. By generating C57BL/6J-backcrossed Nmu/Nms/Gpr176 triple knockout mice, we noted that the mutant mice had a greater magnitude of phase shift in response to early subjective night light than wildtype mice, while Nmu/Nms double knockout mice as well as Gpr176 knockout mice are normal in the phase shifts induced by light. At the molecular level, Nmu -/- Nms -/- Gpr176 -/- mice had a reduced induction of Per1 and cFos mRNA expression in the SCN by light and mildly upregulated circadian expression of Per2, Prok2, Rgs16, and Rasl11b. These expressional changes may underlie the phenotype of the Nmu/Nms/Gpr176 knockout mice. Our data argue that there is a mechanism requiring Nmu, Nms, and Gpr176 for the proper modulation of light-induced phase shift in mice. Simultaneous modulation of Nmu/Nms/Gpr176 may provide a potential target option for modulating the circadian clock.